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Transcriptomic characterization of Wild type mouse Embryonic Stem Cells (mESCs), β-actin Knock out mESC and upon rescue with a nuclear localization signal β-actin

ABSTRACT: Pluripotency and lineage commitment in embryonic stem cells depend on coordinated regulation of chromatin architecture and extracellular matrix (ECM) signaling. Here, we identify nuclear β-actin as a key regulator linking these processes in mouse embryonic stem cells. Loss of β-actin disrupts core pluripotency factors, including Oct4 and Sox2, and causes broad transcriptional changes, while nuclear re-expression rescues these defects. Chromatin accessibility analysis revealed reduced accessibility at regulatory regions of pluripotency genes, consistent with impaired chromatin remodeling. β-actin depletion also altered ECM-related gene expression, matrix properties, and cellular biomechanics, leading to impaired self-renewal, skewed lineage specification, and defective differentiation, particularly reduced neuronal potential and increased mesodermal-like fate bias. In vivo, β-actin loss restricted teratoma growth and compromised tri-lineage differentiation. Together, these results define nuclear β-actin as an important regulator of chromatin accessibility, ECM-dependent signaling, and stem cell fate.

ORGANISM(S): Mus musculus

PROVIDER: GSE327304 | GEO | 2026/04/13

REPOSITORIES: GEO

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Transcriptomic and Accessibilty characterization of Wild type mouse Embryonic Stem Cells (mESCs), β-actin Knock out mESC and upon rescue with a nuclear localization signal β-actin

Project description:Pluripotency and lineage commitment in embryonic stem cells depend on coordinated regulation of chromatin architecture and extracellular matrix (ECM) signaling. Here, we identify nuclear β-actin as a key regulator linking these processes in mouse embryonic stem cells. Loss of β-actin disrupts core pluripotency factors, including Oct4 and Sox2, and causes broad transcriptional changes, while nuclear re-expression rescues these defects. Chromatin accessibility analysis revealed reduced accessibility at regulatory regions of pluripotency genes, consistent with impaired chromatin remodeling. β-actin depletion also altered ECM-related gene expression, matrix properties, and cellular biomechanics, leading to impaired self-renewal, skewed lineage specification, and defective differentiation, particularly reduced neuronal potential and increased mesodermal-like fate bias. In vivo, β-actin loss restricted teratoma growth and compromised tri-lineage differentiation. Together, these results define nuclear β-actin as an important regulator of chromatin accessibility, ECM-dependent signaling, and stem cell fate.

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ATAC-Seq analysis of beta actin knockout mouse embryonic fibroblasts expressing NLS-tagged beta-actin

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Project description:Actin and nuclear myosin 1 (NM1) are emerging as regulators of transcription and chromatin organization. Using a genome-wide approach we report here that β-actin binds both intergenic and genic regions across the entire mammalian genome, associated with both protein-coding and rRNA genes. Across the rDNA transcription unit the distribution of β-actin correlated with NM1 and the other subunits of the B-WICH complex, WSTF and SNF2h. In β-actin-/- mouse embryonic fibroblasts (MEFs), we found that rRNA synthesis levels are down-regulated concomitantly with drops in Pol I and NM1 occupancies across the rRNA gene. In knock-in experiments, reintroduction of wild-type β-actin but not mutated forms with polymerization defects, rescued rRNA synthesis underscoring the direct role for β-actin in Pol I transcription and the importance of polymerization during the transcription process. The rRNA defects in the β-actin-/-MEFs are accompanied by epigenetic reprogramming that leads to up-regulation of the repressive mark H3K4me1. In addition, a high resolution chromatin accessibility assay showed that the absence of β-actin leads to a more compact chromatin at specific locations, including promoter-proximal enhancer (T0 sequence) and Sal boxes (T1-T10), disturbing binding of the transcription termination factor 1 (TTF1). We propose a novel mechanism where the polymerase-associated β-actin synergizes with NM1 to coordinate the establishment of permissive chromatin with the correct rDNA topology for Pol I transcription enhancement.

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